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Background Lymphedema is a common problem that adversely impacts quality of life in breast cancer survivors. Although lymphedema risk is modifiable through behavior change, there is no standardized approach to educate survivors about risk-lowering strategies. Furthermore, misconceptions about lymphedema risk factors and risk-lowering strategies are common. The aim of this study was to evaluate the effect of lymphedema therapy referral on knowledge about lymphedema risk. Methods This was a cross-sectional single institution study in which breast cancer survivors at a National Cancer Institute-designated cancer center completed an anonymous questionnaire between 2014 and 2015. Eligibility criteria were age ≥ 18, female sex, English-speaking, > 6 months post definitive breast cancer surgery, no cancer recurrence, and no prior or subsequent second cancer. The questionnaire included sociodemographic variables, clinical factors including prior lymphedema therapy referral, and 10 true/false questions assessing knowledge about lymphedema risk. Multivariable logistic regression analyses assessed the relationship between prior lymphedema therapy referral and correctly answering questions about lymphedema risk. Results Of 209 participants, 53 (25%) had been referred to lymphedema therapy. Those who had undergone sentinel lymph node biopsy were less frequently referred to lymphedema therapy [15 (14%)] than those who had undergone axillary lymph node dissection [38 (39%)]. Five of the true/false questions had a correct response rate of < 80%. After controlling for age, race/ethnicity, education, type of axillary surgery, and receipt of radiation therapy, referral for lymphedema therapy was associated with correctly answering two questions about lymphedema: weight gain increases lymphedema risk [odds ratio, 95% confidence interval: 3.63 (1.66–7.96)] and patients are recommended to exercise their arm on an airplane [2.65 (1.15–6.13)]. Conclusions Misconceptions about lymphedema prevention and management are common among breast cancer survivors. Lymphedema therapy referral is a potential opportunity to debunk misunderstandings and educate at-risk patients regarding lymphedema.

After injury to the corticospinal tract (CST) in early development there is large-scale adaptation of descending motor pathways. Some studies suggest the uninjured hemisphere controls the impaired forelimb, while others suggest that the injured hemisphere does; these pathways have never been compared directly. We tested the contribution of each motor cortex to the recovery forelimb function after neonatal injury of the CST. We cut the left pyramid (pyramidotomy) of postnatal day 7 rats, which caused a measurable impairment of the right forelimb. We used pharmacological inactivation of each motor cortex to test its contribution to a skilled reach and supination task. Rats with neonatal pyramidotomy were further impaired by inactivation of motor cortex in both the injured and the uninjured hemispheres, while the forelimb of uninjured rats was impaired only from the contralateral motor cortex. Thus, inactivation demonstrated motor control from each motor cortex. In contrast, physiological and anatomical interrogation of these pathways support adaptations only in the uninjured hemisphere. Intracortical microstimulation of motor cortex in the uninjured hemisphere of rats with neonatal pyramidotomy produced responses from both forelimbs, while stimulation of the injured hemisphere did not elicit responses from either forelimb. Both anterograde and retrograde tracers were used to label corticofugal pathways. There was no increased plasticity from the injured hemisphere, either from cortex to the red nucleus or the red nucleus to the spinal cord. In contrast, there were very strong CST connections to both halves of the spinal cord from the uninjured motor cortex. Retrograde tracing produced maps of each forelimb within the uninjured hemisphere, and these were partly segregated. This suggests that the uninjured hemisphere may encode separate control of the unimpaired and the impaired forelimbs of rats with neonatal pyramidotomy.

OBJECTIVES/GOALS: There is a high burden of lung cancer in persons living with HIV (PLWH). The role that HIV status, by levels of immune function and viral load, has on survival from lung cancer is not fully understood. The study’s objectives were to assess 1) the association of HIV with survival in non-small cell lung cancer (NSCLC) and 2) prognostic factors in PLWH with NSCLC. METHODS/STUDY POPULATION: Participants were from a cohort of lung cancer patients diagnosed between 2004-2017 in the Bronx, NY, with vital status ascertainment at least annually. We compared survival from NSCLC diagnosis between HIV-negative patients (HIV-, N = 2881) and PLWH (N = 88), using Cox regression, accounting for clinical and sociodemographic factors including smoking status. In three separate comparisons to HIV-, PLWH were dichotomized by CD4 count (<200 vs. ≥200 cells/μL), CD4/CD8 ratio (median, <0.43 vs. ≥0.43) and HIV viral load (VL) suppression (<75 vs. ≥75 copies/mL). In PLWH only, we assessed the relationships of CD4 count, CD4/CD8 ratio, and VL at diagnosis with survival adjusting for age, sex, and cancer stage. CD4 count and CD4/CD8 ratio were also examined as time-varying variables using a counting process approach. RESULTS/ANTICIPATED RESULTS: PLWH were younger (median 56 years, IQR 51-52 vs. 68, IQR 60-76) and more likely to be current smokers (58% vs. 37%) at diagnosis than HIV- patients. Median survival was lower in PLWH [1.1 years, 95% confidence interval (95%CI): 0.6-1.3] than in HIV- [1.6 (1.5-1.7)]. Survival comparing PLWH with higher CD4/CD8 to HIV- was similar [hazard ratio (HR), 95%CI: 0.63 (0.37-1.07)], but those with lower CD4/CD8 experienced worse survival (HR = 1.74, 95%CI: 1.07-3.89). Among PLWH, having a CD4 count < 200 cells/μL was associated with over twice the risk of death compared to those with CD4 ≥ 200 cells/μL (HR = 2.37, 95%CI: 1.14-4.92). VL and CD4/CD8 ratio were not associated with survival. Lower time-updated CD4 count was also associated with worse survival (HR = 2.19 for CD4 <200 vs. >200 cells/μL, 95%CI: 1.16-4.13). DISCUSSION/SIGNIFICANCE OF IMPACT: Among persons with NSCLC, CD4/CD8 ratio nearest diagnosis was shown to distinguish mortality risk in PLWH compared with HIV- patients. In addition, PLWH with low CD4 had worse prognosis than PLWH who had higher CD4 counts. These results suggest HIV immune status to be an essential component influencing survival in lung cancer.

[This corrects the article DOI: 10.3389/fncir.2018.00028.].

Purpose Lung cancer mortality has been shown to vary by race and ethnicity in cancer registries; however, studies often do not account for smoking status. We sought to summarize the independent contribution of race and ethnicity to survival in US lung cancer patients, accounting for important variables including smoking status. Methods PubMed was used to identify 1,877 potentially eligible studies of which 27 were included. Studies were excluded if they did not account for age, race and/or ethnicity, and smoking status. Fixed- and random-effects meta-analyses were conducted using the reported adjusted hazard ratios (HR) of Hispanic ethnicity and Asian and African-American race compared to Non-Hispanic whites (NHWs) on overall survival in lung cancer. Results Hispanic ethnicity and Asian race were associated with decreased adjusted risk of death (Hispanic: N studies  = 5, N subjects  = 108,810, HR = 0.95, 95% CI 0.90–1.00; Asian: N studies  = 6, N subjects  = 128,950, HR = 0.86, 95% CI 0.81–0.90). The results were similar when excluding studies of solely never-smokers. There was no significant difference in survival between African-American and white race after adjustment ( N studies  = 10, N subjects  = 131,378, HR = 0.98, 95% CI 0.96–1.01). Other prognostic factors were female gender (HR = 0.88, 95% CI 0.87–0.89), unmarried status (HR = 1.08, 95% CI 1.04–1.11), ever-smoking status (HR = 1.11, 95% CI 1.08–1.15), having comorbidities (HR = 1.39, 95% CI 1.24–1.56), and treatment receipt (surgery: HR = 0.33, 95% CI 0.32–0.34; radiation: HR = 0.87, 95% CI 0.85–0.88; chemotherapy: HR = 0.64, 95% CI 0.63–0.65). Conclusions Even after adjustment for clinical factors and smoking status, Hispanics and Asians experienced improved survival compared to NHWs. Future studies are needed to elucidate the drivers of these survival disparities.

Household air pollution (HAP) is of public health concern, with ~3 billion people worldwide (including >15 million in the US) exposed. HAP from coal use is a human lung carcinogen, yet the epidemiological evidence on carcinogenicity of HAP from biomass use, primarily wood, is not conclusive. To robustly assess biomass’s carcinogenic potential, prospective studies of individuals experiencing a variety of HAP exposures are needed. We have built a global consortium of 13 prospective cohorts (HAPCO: Household Air Pollution Consortium) that have site- and disease-specific mortality and solid fuel use data, for a combined sample size of 587,257 participants and 57,483 deaths. HAPCO provides a novel opportunity to assess the association of HAP with lung cancer death while controlling for important confounders such as tobacco and outdoor air pollution exposures. HAPCO is also uniquely positioned to determine the risks associated with cancers other than lung as well as nonmalignant respiratory and cardiometabolic outcomes, for which prospective epidemiologic research is limited. HAPCO will facilitate research to address public health concerns associated with HAP-attributed exposures by enabling investigators to evaluate sex-specific and smoking status-specific effects under various exposure scenarios.

ObjectiveTo prospectively investigate whether diversity in oral microbiota is associated with risk of lung cancer among never-smokers.Design and settingA nested case–control study within two prospective cohort studies, the Shanghai Women’s Health Study (n=74 941) and the Shanghai Men’s Health Study (n=61 480).ParticipantsLifetime never-smokers who had no cancer at baseline. Cases were subjects who were diagnosed with incident lung cancer (n=114) and were matched 1:1 with controls on sex, age (≤2 years), date (≤30 days) and time (morning/afternoon) of sample collection, antibiotic use during the week before sample collection (yes/no) and menopausal status (for women).Main outcomes and measuresMetagenomic shotgun sequencing was used to measure the community structure and abundance of the oral microbiome in pre-diagnostic oral rinse samples of each case and control. Multivariable logistic regression models were used to estimate the association of lung cancer risk with alpha diversity metrics and relative abundance of taxa. The Microbiome Regression-Based Kernel Association Test (MiRKAT) evaluated the association between risk and the microbiome beta diversity.ResultsSubjects with lower microbiota alpha diversity had an increased risk of lung cancer compared with those with higher microbial alpha diversity (Shannon: ptrend=0.05; Simpson: ptrend=0.04; Observed Species: ptrend=0.64). No case–control differences were apparent for beta diversity (pMiRKAT=0.30). After accounting for multiple comparisons, a greater abundance of Spirochaetia (ORlow 1.00 (reference), ORmedium 0.61 (95% CI 0.32 to 1.18), ORhigh 0.42 (95% CI 0.21 to 0.85)) and Bacteroidetes (ORlow 1.00 (reference), ORmedium 0.66 (95% CI 0.35 to 1.25), ORhigh 0.31 (95% CI 0.15 to 0.64)) was associated with a decreased risk of lung cancer, while a greater abundance of the Bacilli class (ORlow 1.00 (reference), ORmedium 1.49 (95% CI 0.73 to 3.08), ORhigh 2.40 (95% CI 1.18 to 4.87)) and Lactobacillales order (ORlow 1.00 (reference), ORmedium 2.15 (95% CI 1.03 to 4.47), ORhigh 3.26 (95% CI 1.58 to 6.70)) was associated with an increased risk of lung cancer.ConclusionsOur prospective study of never-smokers suggests that lower alpha diversity was associated with a greater risk of lung cancer and the abundance of certain specific taxa was associated with altered risk, providing further insight into the aetiology of lung cancer in the absence of active tobacco smoking.

Hispanic/Latino ethnicity is associated with improved survival from non-small cell lung cancer compared to that for non-Hispanic Whites even though Hispanics/Latinos are more likely to potentially have inferior access-to-care and experience greater health disparities. To this end, we conducted a literature review to identify possible explanations for this survival benefit, including the role of chronic obstructive pulmonary disease and cardiovascular diseases, genetic variation, cultural influences, and immigration factors. Overall, intermittent smoking patterns, genetic variation, co-morbidities, and cultural influences were all factors likely to partially explain this survival benefit. On the other hand, immigration factors, acculturation, and access-to-care were less likely to support the survival advantage. Future research should analyze relevant Hispanic/Latino subgroups (e.g., Mexican, Puerto Rican, Cuban, Dominican, Central American, South American) and specifically focus on the relationship between Hispanic/Latino ethnicity and different lung cancer subtypes. If the Hispanic/Latino mortality benefit observed in lung cancer truly exists, a better understanding of the underlying mechanism(s) may help extend these benefits to other ethnic and racial groups.

Background Hispanics/Latinos are a growing yet understudied population in the United States (US). Despite lower socioeconomic status, Hispanics/Latinos tend to have similar or better health outcomes than Non-Hispanic Whites (NHWs). This phenomenon has not been conclusively studied for lung cancer. Methods Using a cohort of patients at Montefiore Medical Center (MMC) in the Bronx, NY, we examined factors related to lung cancer survival by race/ethnicity with an emphasis on Hispanics/Latinos. Subjects were diagnosed with non-small cell lung cancer (NSCLC) between 2004 and 2017. Demographic and clinical data were obtained from MMC’s clinical systems and tumor-related information from MMC/Einstein’s Cancer Registry. Survival was assessed using Cox proportional hazards modeling adjusted for clinical and sociodemographic factors including smoking. Factors related to survival within each major racial/ethnic group were examined. Results Hispanics/Latinos experienced decreased risk of death relative to NHWs [hazard ratio (HR) = 0.70, 95% confidence interval (95%CI) 0.57–0.86] overall and by sex (males: HR = 0.78, 95%CI 0.59–1.03, females: HR = 0.61, 95%CI 0.44–0.86). Decreased risk among Hispanics/Latinos relative to NHWs was evident in never-smokers (HR = 0.55, 95%CI 0.29–1.01), ever-smokers (HR = 0.72, 95%CI 0.57–0.90), younger subjects (HR = 0.73, 95%CI 0.54–0.99), and older subjects (HR = 0.72, 95%CI 0.53–0.97). Surgery was associated with improved survival in Hispanics/Latinos (HR = 0.60, 95%CI 0.43–0.85), and smoking with worse survival (HR = 1.56, 95%CI 1.02–2.39). Survival did not differ between Non-Hispanic Blacks and NHWs. Conclusions In a poor urban community, Hispanics/Latinos experience improved survival from NSCLC compared to NHWs, which is not entirely explained by smoking. Future research should investigate the drivers of this benefit and differences in survival by Hispanic/Latino origin.

Background: Hispanics/Latinos represent >15% of the United States (US) population and experience a high burden of cardiovascular disease (CVD) and diabetes. Dietary exposure, particularly to arsenic (As), may be associated with CVD and diabetes in Hispanics/Latinos. Rural populations in the US exposed to As in drinking water have increased risk of diabetes and CVD; however, little is known about the risk among urban populations with low As in water who are mostly exposed to As through food. Methods: To explore the levels of inorganic arsenic exposure (the sum of inorganic and methylated arsenic species in urine, ∑As, corrected by a residual-based method) in persons of Hispanic/Latino origin, we conducted a pilot study quantifying urinary arsenic levels among 45 participants in the Study of Latinos: Nutrition & Physical Activity Assessment Study (SOLNAS). Results: The median (interquartile range) of the urinary arsenic species (µg/L) were as follows: inorganic As 0.6 (0.4, 1.0), monomethylarsonic acid 1.2 (0.7, 1.9), dimethylarsinic acid 7.2 (4.3, 15.3), and ∑As 6.0 (4.3, 10.5). Conclusions: This study adds to the existing evidence that harmful forms of arsenic are present in this group of Hispanics/Latinos.